Figure 4.

Diagram illustrating the different signaling cascades and targets underpinning S-RNase-mediated pollen tube inhibition and PCD in Pyrus. (1) S-RNases (blue polygon) enter the growing pollen tube by ABC transporters or via vesicle trafficking. Self S-RNases are not recognized by the SLF^SCF complex and are allowed to interact with multiple targets inside the pollen tube. (2) Self S-RNase interacts with and inhibits phospholipase C (PLC), leading to a decreased production of IP3 which in its turn reduces Ca²⁺ import through Ca²⁺ channels. This reduced Ca²⁺ uptake leads to the mitigation of the Ca²⁺ gradient in the pollen tube tip, inhibiting pollen tube growth. (3) Self S-RNases stimulate the expression of phospholipase D (PLD), which stimulates production of phosphatidic acid (PPa). PPa can temporarily delay actin depolymerization in pollen tubes, providing a first defensive mechanism against pollen tube growth inhibition. (4) However, self S-RNases can also interact directly with F-actin, causing actin depolymerization and leading to pollen tube growth inhibition. (5) Self S-RNases can physically interact with pyrophosphatases (PPases), and thereby inhibit their activity. This leads to the accumulation of inorganic pyrophosphate (PPi) which also causes reduced pollen tube growth. (6) Upon challenge with self S-RNases, the mitochondrial membrane collapses, causes leakage of cytochrome c into the cytosol and a cessation of H₂O₂ production. The presence of self S-RNases in the pollen tube also reduces NADPH levels, causing a decrease in plasma membrane ROS formation. As a result, tip-localized ROS accumulation is disrupted, providing another trigger for induction of PCD. (7) Challenge with self S-RNases has also been shown to cause RNA degradation and nuclear DNA degradation, two processes that are also linked to programmed cell death (PCD). Question marks denote processes in which the exact role of the S-RNase still needs to be elucidated.